Viral-Mediated mRNA Degradation for Pathogenesis

Du, Shujuan; Liu, Xiaoqing; Cai, Qiliang

doi:10.3390/biomedicines6040111

Cited by 3 publications

(6 citation statements)

References 69 publications

(77 reference statements)

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“…Various deadenylation‐dependent or deadenylation‐independent mechanisms commonly regulate mRNA degradation [21–23]. Viral mRNA degradation has evolved to become a primal host antipathogen mechanism [24–27]. To circumvent this host strategy, viral self‐defense entails avoiding presentation of AU‐rich elements (AREs) and GU‐rich elements (GUEs), motifs that engage mRNA degradation pathways via interactions with pathway ARE‐ or GRE‐binding proteins, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…Many viral strategies designed to manipulate host RNA degradation machineries evolved to create a high viral mRNA burden during the host infection. Relying on the use of strong promoters, viral transcripts are generated at higher rates than are host transcripts, resulting in viral transcript enrichment and, subsequently, a higher viral protein production load [24,25]. Thus, we studied endogenous degradation motifs in coronaviruses, particularly in their putative 3′‐ and 5′‐UTR sequences, to understand the roles of such motifs in the high viral load associated with coronaviral infections.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, we found that coronaviruses contain mostly AT‐rich rather than GT‐rich motifs (Table S6). This might reflect processing by predominately AT‐dependent degradation mechanisms [25]. Moreover, in HIV, as well as in SARS‐CoV‐2, highly expressed genes adopt nonoptimal codon usage (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Non‐optimal codon usage preferences of coronaviruses determine their promiscuity for infecting multiple hosts

et al. 2021

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Circulating animal coronaviruses occasionally infect humans. The SARS‐CoV‐2 is responsible for the current worldwide outbreak of COVID‐19 that has resulted in 2 112 844 deaths as of late January 2021. We compared genetic code preferences in 496 viruses, including 34 coronaviruses and 242 corresponding hosts, to uncover patterns that distinguish single‐ and ‘promiscuous’ multiple‐host‐infecting viruses. Based on a codon usage preference score, promiscuous viruses were shown to significantly employ nonoptimal codons, namely codons that involve ‘wobble’ binding to anticodons, as compared to single‐host viruses. The codon adaptation index (CAI) and the effective number of codons (ENC) were calculated for all viruses and hosts. Promiscuous viruses were less adapted hosts vs single‐host viruses (P‐value = 4.392e‐11). All coronaviruses exploit nonoptimal codons to infect multiple hosts. We found that nonoptimal codon preferences at the beginning of viral coding sequences enhance the translational efficiency of viral proteins within the host. Finally, coronaviruses lack endogenous RNA degradation motifs to a significant degree, thereby increasing viral mRNA burden and infection load. To conclude, we found that promiscuously infecting coronaviruses prefer nonoptimal codon usage to remove degradation motifs from their RNAs and to dramatically increase their viral RNA production rates.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Non‐optimal codon usage preferences of coronaviruses determine their promiscuity for infecting multiple hosts

et al. 2021

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“…Several stresses, including viral infection, cause a deregulation of cellular mRNA surveillance. Viruses hijack the host translation machinery to create a cellular environment suitable for their translation and replication ( 91 ). Conversely, proteins involved in mRNA degradation, including decapping enzymes and exonucleases, can be used to restrict viral infection ( 92 ).…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomics of Ostreid Herpesvirus 1 and Pacific Oyster Interactions With Two Families Exhibiting Contrasted Susceptibility to Viral Infection

Leprêtre

Faury²,

Segarra

et al. 2021

Front. Immunol.

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Massive mortality outbreaks affecting Pacific oysters (Crassostrea gigas) spat/juveniles are often associated with the detection of a herpesvirus called ostreid herpesvirus type 1 (OsHV-1). In this work, experimental infection trials of C. gigas spat with OsHV-1 were conducted using two contrasted Pacific oyster families for their susceptibility to viral infection. Live oysters were sampled at 12, 26, and 144 h post infection (hpi) to analyze host-pathogen interactions using comparative proteomics. Shotgun proteomics allowed the detection of seven viral proteins in infected oysters, some of them with potential immunomodulatoy functions. Viral proteins were mainly detected in susceptible oysters sampled at 26 hpi, which correlates with the mortality and viral load observed in this oyster family. Concerning the Pacific oyster proteome, more than 3,000 proteins were identified and contrasted proteomic responses were observed between infected A- and P-oysters, sampled at different post-injection times. Gene ontology (GO) and KEGG pathway enrichment analysis performed on significantly modulated proteins uncover the main immune processes (such as RNA interference, interferon-like pathway, antioxidant defense) which contribute to the defense and resistance of Pacific oysters to viral infection. In the more susceptible Pacific oysters, results suggest that OsHV-1 manipulate the molecular machinery of host immune response, in particular the autophagy system. This immunomodulation may lead to weakening and consecutively triggering death of Pacific oysters. The identification of several highly modulated and defense-related Pacific oyster proteins from the most resistant oysters supports the crucial role played by the innate immune system against OsHV-1 and the viral infection. Our results confirm the implication of proteins involved in an interferon-like pathway for efficient antiviral defenses and suggest that proteins involved in RNA interference process prevent viral replication in C. gigas. Overall, this study shows the interest of multi-omic approaches applied on groups of animals with differing sensitivities and provides novel insight into the interaction between Pacific oyster and OsHV-1 with key proteins involved in viral infection resistance.

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“…78 The relationship between the virus and Dcp2 implies that the virus is controlling host mRNA degradation to inhibit the antiviral immune response. 79 F I G U R E 4 Schematic diagram of the bunyavirus RNA capping mechanism.…”

Section: Cytoplasmic Replicating Virusesmentioning

confidence: 99%

Viral RNA capping: Mechanisms and antiviral therapy

Chen,

Jiang,

et al. 2024

Journal of Medical Virology

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RNA capping is an essential trigger for protein translation in eukaryotic cells. Many viruses have evolved various strategies for initiating the translation of viral genes and generating progeny virions in infected cells via synthesizing cap structure or stealing the RNA cap from nascent host messenger ribonucleotide acid (mRNA). In addition to protein translation, a new understanding of the role of the RNA cap in antiviral innate immunity has advanced the field of mRNA synthesis in vitro and therapeutic applications. Recent studies on these viral RNA capping systems have revealed startlingly diverse ways and molecular machinery. A comprehensive understanding of how viruses accomplish the RNA capping in infected cells is pivotal for designing effective broad‐spectrum antiviral therapies. Here we systematically review the contemporary insights into the RNA‐capping mechanisms employed by viruses causing human and animal infectious diseases, while also highlighting its impact on host antiviral innate immune response. The therapeutic applications of targeting RNA capping against viral infections and the development of RNA‐capping inhibitors are also summarized.

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Viral-Mediated mRNA Degradation for Pathogenesis

Cited by 3 publications

References 69 publications

Non‐optimal codon usage preferences of coronaviruses determine their promiscuity for infecting multiple hosts

Non‐optimal codon usage preferences of coronaviruses determine their promiscuity for infecting multiple hosts

Comparative Proteomics of Ostreid Herpesvirus 1 and Pacific Oyster Interactions With Two Families Exhibiting Contrasted Susceptibility to Viral Infection

Viral RNA capping: Mechanisms and antiviral therapy

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